Lab-on-a-Molecule Probe: Multitarget Detection of Five Aromatic Pesticides Using a Supramolecular Probe under Single Wavelength Excitation.

In order to prevent and control the effects of pesticide residues on human health and the ecological environment, the rapid, highly sensitive, and selective detection of multiple pesticide residues has become an urgent problem to be solved. Herein, a lab-on-a-molecule probe based on a host-guest complex (ThT@Q[8] probe) has been developed to simultaneously analyze multiple aromatic pesticides under single wavelength excitation, such as fuberidazole, thiabendazole, carbendazim, thidiazuron, and tricyclazole. The fluorescence titration spectra of the ThT@Q[8] probe with the five pesticides mentioned above showed that the fluorescence intensity exhibited a good linear correlation with the pesticide concentration and the limit of detection was as low as 10 M.

miR-15a-5p regulates myocardial fibrosis in atrial fibrillation by targeting Smad7.

Background: At present, there is no effective treatment for myocardial fibrosis in atrial fibrillation (AF). It is reported that miR-15a-5p is abnormally expressed in AF patients but its specific role remains unclear. This study aims to investigate the effect of miR-15a-5p in myocardial fibrosis.

Prediction of spontaneous closure of isolated ventricular septal defects in utero and postnatal life.

Background: Ventricular septal defect (VSD) is a highly prevalent fetal congenital heart defect, which can become spontaneously closed during infancy. The current study aims to characterize fetal VSDs that were subsequently spontaneously closed in the first 2 years of life in eastern China.

Methods: Between January 2011 and December 2013, 257 fetal patients diagnosed with isolated VSD by fetal echocardiography at Nanjing Maternity and Child Health Care Hospital, China, were enrolled in the study.

[Interaction of Cucurbit[8]uril with β-Indoleacetic Acid and Methylviologen].

The interaction between Q[8] with β-indoleacetic acid and the methylviologen was studied in aqueous solution with electronic absorption spectroscopy (UV-Vis), fluorescence spectroscopy, 1H NMR spectroscopy and isothermal titration calorimetry (ITC) in details. The authors explored the mode of action, action site and thermodynamic properties of the host-guest system. The electronic absorption and fluorescence spectroscopy data showed that the Q[8]/IAA system and Q[8]/MV²⁺ system informed 1:1 inclusion complexes in aqueous solution.

Effect of LYRM1 knockdown on proliferation, apoptosis, differentiation and mitochondrial function in the P19 cell model of cardiac differentiation in vitro.

To explore the effects of LYRM1 knockdown on proliferation, apoptosis, differentiation and mitochondrial function in the embryonic carcinoma (P19) cell model of cardiac differentiation. Knockdown of LYRM1 using small interfering RNA (siRNA) was confirmed by quantitative real-time PCR. Cell Counting Kit-8(CCK-8) proliferation assays and cell cycle analysis demonstrated that LYRM1 gene silencing significantly inhibited P19 cell proliferation.

Dynamic mitochondrial changes during differentiation of P19 embryonic carcinoma cells into cardiomyocytes.

Murine P19 embryonal carcinoma cells are multipotent cells that can differentiate into cardiomyocytes when treated with dimethyl sulfoxide. This experimental model provides an invaluable tool to study different aspects of cardiac differentiation, such as the function of cardiac‑specific transcription factors and signaling pathways, and the regulation of contractile protein expression. The role of mitochondria during cardiac differentiation is unclear.

Identification of differentially expressed genes involved in transient regeneration of the neonatal C57BL/6J mouse heart by digital gene expression profiling.

Accumulating evidence has revealed that the mammalian heart possesses a measurable capacity for renewal. Neonatal mice retain a regenerative capacity over a short time-frame (≤6 days), but this capacity is lost by 7 days of age. In the present study, differential gene expression profiling of mouse cardiac tissue was performed to further elucidate the mechanisms underlying this process.

Long noncoding RNAs expression profile of the developing mouse heart.

Long noncoding RNAs (lncRNAs) represent a sub-group of noncoding RNAs that are longer than 200 nucleotides. The characterization of lncRNAs and their acceptance as crucial regulators of numerous developmental and biological pathways have suggested that the lncRNA study has gradually become one of the hot topics in the field of RNA biology. Many lncRNAs show spatially and temporally restricted expression patterns during embryogenesis and organogenesis.

Silencing of FABP3 leads to apoptosis-induced mitochondrial dysfunction and stimulates Wnt signaling in zebrafish.

Fatty acid binding protein 3 (FABP3, also termed heart-type fatty acid binding protein) is a member of the intracellular lipid-binding protein family that may be essential in fatty acid transport, cell growth, cellular signaling and gene transcription. Previously, we demonstrated that FABP3 was involved in apoptosis-associated congenital cardiac malformations; however, its mechanism of regulation remains unclear. Apoptosis has increasingly been considered to be important in cardiac development.

Overexpression of FABP3 promotes apoptosis through inducing mitochondrial impairment in embryonic cancer cells.

Fatty acid-binding protein 3 (FABP3) is a low-molecular-weight protein with a distinct tissue distribution that may play an important role in fatty acid transport, cell growth, cellular signaling, and gene transcription. Previously, we have found that FABP3 was involved in apoptosis-associated congenital cardiac malformations, but the underlying mechanisms have not yet been described. In the present study, we investigated the characteristics of mitochondrial dysfunction in embryonic cancer cells (P19 cells) that overexpressed FABP3.

Silencing of FABP3 promotes apoptosis and induces mitochondrion impairment in embryonic carcinoma cells.

Fatty acid binding protein 3 (FABP3) (also known as H-FABP) is a member of the intracellular lipid-binding protein family, and is mainly expressed in cardiac muscle tissue. The in vivo function of FABP3 is proposed to be in fatty acid metabolism, trafficking, and cell signaling. Our previous study found that FABP3 is highly regulated in patients with ventricular septal defect (VSD), and may play a significant role in the development of human VSD.